Chapter 5BASIC IMMUNOLOGY

BYDR. UCHE AMAEFUNA-OBASI

THERE ARE MORE TO LECTURES THAN JUST SLIDES

Definition;• It is the branch of medicine and biology which

is concerned with immunity.

IMMUNITY;• This is the ability of an organism to resist a

particular infection or toxin by the action of specific antibodies or sensitized white blood cells.

IMMUNE SYSTEM• The immune system is designed to protect the

body from harmful diseases. • The immune system begins to develop in the

embryo and by the time the baby is born, it is a sophisticated collection of tissues that includes the blood, lymphatic system, thymus, spleen, skin, and mucosa.

• The immune system responds to any antigen, whether is it harmless, like grass pollen, or harmful, such as a virus or bacterial infection.

• Everyone’s immune system is different, and reacts differently to every antigen.

OVER VIEW• The immune system is designed to defend the

body against foreign or dangerous invaders. Such invaders include;

• Microorganisms (commonly called germs, such as bacteria, viruses, and fungi)

• Parasites (such as worms)• Cancer cells• Even transplanted organs and tissue

• To defend the body against these invaders, the immune system must be able to distinguish between

• What belongs in the body (self)• What does not (non-self or foreign)• Any substances that are identified as non-self,

particularly if they are perceived as dangerous (for example, if they can cause disease), stimulate an immune response in the body. Such substances are called antigens.

• Antigens may be contained within or on bacteria, viruses, other microorganisms, or cancer cells. Antigens may also exist on their own—for example, as food molecules or pollen.

• A normal immune response consists of recognizing a potentially harmful foreign antigen, activating and mobilizing forces to defend against it, and attacking it.

• If the immune system malfunctions and mistakes self for non-self, it may attack the body’s own tissues, causing an autoimmune disorder, such as rheumatoid arthritis, thyroiditis, or systemic lupus erythematosus (lupus).

UNDERSTANDING THE IMMUNE SYSTEM• Antibody (immunoglobulin): A protein that is

produced by B cells and that tightly binds to the antigen of an invader, tagging the invader for attack or directly neutralizing it.

• Antigen: Any substance that the immune system can recognize and can thus stimulate an immune response.

• B cell (B lymphocyte): A white blood cell that produces antibodies specific to the antigen that stimulated their production.

• Basophil: A white blood cell that releases histamine (a substance involved in allergic reactions) and that produces substances to attract other white blood cells (neutrophils and eosinophils) to a trouble spot.

• Cell: The smallest unit of a living organism, composed of a nucleus and cytoplasm surrounded by a membrane.

• Chemotaxis: The process of using a chemical substance to attract cells to a particular site.

• Complement system: A group of proteins that are involved in a series of reactions (called the complement cascade) designed to defend the body.

E.g by killing bacteria and other foreign cells, making foreign cells easier for macrophages to identify and ingest, and attracting macrophages and neutrophils to a trouble spot.

• Cytokines: Proteins that are secreted by immune and other cells that act as the immune system’s messengers to help regulate an immune response.

• Dendritic cell: A cell that is derived from white blood cells, resides in tissues, and helps T cells recognize foreign antigens.

• Eosinophil: A white blood cell that kills bacteria, that kills other foreign cells too big to ingest, that may help immobilize and kill parasites, that participates in allergic reactions, and that may help destroy cancer cells.

• Helper T cell: A white blood cell that helps B cells produce antibodies against foreign antigens, that helps killer T cells become active, and that stimulates macrophages.

• Histocompatibility: Literally, compatibility of tissue. Determined by human leukocyte antigens (see below) and used to determine whether a transplanted tissue or organ will be accepted by the recipient.

• Human leukocyte antigens (HLA): A group of identification molecules that are located on the surface of all cells in a combination that is almost unique for each person, thereby enabling the body to distinguish self from non-self. Also called the major histocompatibility complex.

• Immune complex: An antibody attached to an antigen.• Immune response: The reaction of the immune

system to an antigen.• Immunoglobulin: An antibody.• Interleukin: A type of messenger (cytokine) secreted

by some white blood cells to affect other white blood cells.

• Killer (cytotoxic) T cell: A T cell that attaches to infected cells and cancer cells and kills them.

• Leukocyte: A white blood cell, such as a monocyte, a neutrophil, an eosinophil, a basophil, or a lymphocyte (a B cell or T cell).

• Lymphocyte: The white blood cell responsible for acquired (specific) immunity, including producing antibodies (by B cells), distinguishing self from non-self (by T cells), and killing infected cells and cancer cells (by killer T cells).

• Macrophage: A large cell that develops from a white blood cell called a monocyte, that ingests bacteria and other foreign cells, that helps T cells identify microorganisms and other foreign substances, and that is normally present in the lungs, skin, liver, and other tissues.

• Major histocompatibility complex (MHC): A synonym for human leukocyte antigens.

• Mast cell: A cell in tissues that releases histamine and other substances involved in inflammatory and allergic reactions.

• Molecule: A group of atoms chemically combined to form a unique substance.

• Natural killer cell: A type of white blood cell that can recognize and kill abnormal cells, such as certain infected cells and cancer cells, without having to first learn that the cells are abnormal.

• Neutrophil: A white blood cell that ingests and kills bacteria and other foreign cells.

• Phagocyte: A type of cell (such as a neutrophil or macrophage) that ingests and kills or destroys invading microorganisms, other cells, and cell fragments.

• Phagocytosis: The process of a cell engulfing and ingesting an invading microorganism, another cell, or a cell fragment.

• Receptor: A molecule on a cell’s surface or inside the cell that can identify specific molecules, which fit precisely in it—as a key fits in its lock.

• Regulatory (suppressor) T cell: A white blood cell that helps end an immune response.

• T cell (T lymphocyte): A white blood cell that is involved in acquired immunity and that may be one of three types: helper, killer (cytotoxic), or regulatory.

• Disorders of the immune system • The body generates an immune response against itself

(an autoimmune disorder).• The body cannot generate appropriate immune

responses against invading microorganisms (an immunodeficiency disorder).

• An excessive immune response to often harmless foreign antigens damages normal tissues (an allergic reaction).

The functional importance of the immune system.

TYPES OF IMMUNITY-INNATE/NATURAL.

AQUIRED/ADAPTIVE/SPECIFIC.

• Innate immunity refers to nonspecific defense mechanisms that come into play immediately or within hours of an antigen's appearance in the body. These mechanisms include physical barriers such as skin, chemicals in the blood, and immune system cells that attack foreign cells in the body. The innate immune response is activated by chemical properties of the antigen.

• Innate (natural) immunity is so named because it is present at birth and does not have to be learned through exposure to an invader.

• It thus provides an immediate response to foreign invaders. However, its components treat all foreign invaders in much the same way.

• They recognize only a limited number of identifying substances (antigens) on foreign invaders.

• However, these antigens are present on many different invaders.

• Innate immunity, unlike acquired immunity, has no memory of the encounters, does not remember specific foreign antigens, and does not provide any ongoing protection against future infection.

The white blood cells involved in innate immunity are;

• Monocytes (which develop into macrophages)• Neutrophils• Eosinophils• Basophils• Natural killer cells

Innate immunity

• A hallmark of the innate immune system is that it has no memory of a previous encounter with a foreign organism.

• The system is good at dealing with extracellular bacteria, fungi and intracellular viruses.

• The adaptive immune system, on the other hand, is called into action against pathogens that are able to evade or overcome innate immune defenses.

• Components of the adaptive immune system are normally silent; however, when activated, these components “adapt” to the presence of infectious agents by activating, proliferating, and creating potent mechanisms for neutralizing or eliminating the microbes.

• Acquired (adaptive or specific) immunity is not present at birth.

• It is learned. As a person’s immune system encounters foreign substances (antigens), the components of acquired immunity learn the best way to attack each antigen and begin to develop a memory for that antigen.

• Acquired immunity is also called specific immunity because it tailors its attack to a specific antigen previously encountered. Its hallmarks are its ability to learn, adapt, and remember.

• Acquired immunity takes time to develop after first exposure to a new antigen.

• However afterward, the antigen is remembered, and subsequent responses to that antigen are quicker and more effective than those that occurred after the first exposure.

• The white blood cells responsible for acquired immunity are

• Lymphocytes (T cells and B cells)• Typically, an acquired immune response

begins when antibodies, produced by B cells (B lymphocytes), encounter an antigen.

NOTE: Adaptive immunity• Adaptive immunity refers to antigen-specific

immune response. The adaptive immune response is more complex than the innate.

• The antigen first must be processed and recognized.• Once an antigen has been recognized, the adaptive

immune system creates an army of immune cells specifically designed to attack that antigen.

• Adaptive immunity also includes a "memory" that makes future responses against a specific antigen more efficient.

There are two types of adaptive immune responses:

• humoral immunity, mediated by antibodies produced by B lymphocytes.

• and cell-mediated immunity, mediated by T lymphocytes.

Humoral (Antibody-Mediated) Immunity– Involves production of antibodies against

foreign antigens.– Antibodies are produced by a subset of

lymphocytes called B cells.– B cells that are stimulated will actively

secrete antibodies and are called plasma cells.

– Antibodies are found in extracellular fluids (blood plasma, lymph, mucus, etc.) and the surface of B cells.

– Defense against bacteria, bacterial toxins, and viruses that circulate freely in body fluids, before they enter cells.

– Also cause certain reactions against transplanted tissue.

• Humoral immunity is the immunity in which antibody plays the most important role.

• The cells involved are B cells which differentiate into plasma cells which can excrete antibody.

• B cells need the help of macrophages, T cells, and sometimes complement system, in order to destroy foreign invaders.

Humoral immunity• Results in production of proteins called

“immunoglobulins” or “antibodies”.• Body exposed to “foreign” material termed

“antigen” which may be harmful to body: virus, bacteria, etc.

• Antigen has bypassed other protective mechanisms, i.e, first and second line of defense

Dynamics of Antibody Production.• Antibody production

– Initial antibody produced in IgM– Lasts 10-12 days– Followed by production of IgG– Lasts 4-5 days– Without continued antigenic challenge antibody

levels drop off, although IgG may continue to be produced.

• Secondary Response• Second exposure to SAME antigen.• Memory cells are a beautiful thing.• Recognition of antigen is immediate.• Results in immediate production of protective

antibody, mainly IgG but may see some IgM

• IgG• Most abundant isotype in serum (80%)• Cross placenta and play important role in

protecting fetus– Provides passive immunity to unborn fetus.– Placental cells bind the Fc portion of IgG

and transfer Ab across the placental membrane.

• Activate complement system• Opsonin—phagocytosis

• Crosses placenta – provides baby with immunity for first few weeks of infant’s life.

• Capable of binding complement which will result in cell lysis

• FOUR subclasses – IgG1, IgG2, IgG3 and IgG4

• IgA• Alpha heavy chains• Found in secretions• Produced by lymphoid tissue• Important role in respiratory, urinary and

bowel infections.• 15-10% of Ig pool

• Secretory IgA• Exists as TWO basic structural units, a DIMER• Produced by cells lining the mucous

membranes.

• Does NOT cross the placenta.• Does NOT bind complement.• Present in LARGE quantities in breast milk

which transfers across gut of infant.

• IgM• Mu heavy chains• Largest of all Ig – PENTAMER• 10% of Ig pool• Due to large size restricted to intravascular

space.• FIXES COMPLEMENT.• Does NOT cross placenta.• Of greatest importance in primary immune

response.

• IgE• Epsilon heavy chains• Trace plasma protein• Single structural unit• Fc region binds strongly to mast cells.• Mediates release of histamines and

heparin>allergic reactions• Increased in allergies and parasitic infections.• Does NOT fix complement• Does NOT cross the placenta

• IgD• Delta heavy chains.• Single structural unit.• Accounts for less than 1% of Ig pool.• Primarily a cell bound Ig found on the surface

of B lymphocytes.• Despite studies extending for more than

4 decades, a specific role for serum IgD has not been defined while for IgD bound to the membrane of many B lymphocytes, several functions have been proposed.

• Does NOT cross the placenta.• Does NOT fix complement.

• Types of Humoral ImmunityHumoral immunity can be subdivided into;• Active • Passive immunity. • In active immunity the person actively makes an antibody

after exposure to a foreign antigen. Active immunity can be artificial (e.g., following vaccination

with a live or attenuated virus), or natural (e.g., following exposure to a disease-causing organism).

• In passive immunity a person is given an antibody that has been made by someone else.

It can be artificial (e.g., gamma globulin given to people with agammaglobulinemia) or natural (e.g., maternal antibody that has crossed the placenta into the fetus).

Cell Mediated Immunity– Involves specialized set of lymphocytes called T cells that recognize foreign antigens on the surface

of cells, organisms, or tissues:• Helper T cells• Cytotoxic T cells

– T cells regulate proliferation and activity of other cells of the immune system: B cells, macrophages, neutrophils, etc.

– Defense against:• Bacteria and viruses that are inside host cells

and are inaccessible to antibodies.

• Fungi, protozoa, and helminthes• Cancer cells• Transplanted tissue

IMMUNE SYSTEM DISORDERS WHAT CAN GO WRONG?

• HYPERSENSITIVITY REACTIONS, I-IV• “AUTO”-IMMUNE DISEASES, aka “COLLAGEN”

DISEASES (BAD TERM) Inflammation NOT due to external pathogens, MHC failure.

• IMMUNE DEFICIENCY SYNDROMES, IDS:– PRIMARY (GENETIC)

– SECONDARY (ACQUIRED)

HYPERSENSITIVITY

When the immune systems cause harm to the body, it is referred to as a hypersensitivity.

Four Types of Hypersensitivity Reactions:• Type I (Anaphylactic) Reactions• Type II (Cytotoxic) Reactions• Type III (Immune Complex) Reactions• Type IV (Cell-Mediated) Reactions

1.Anaphylactic hypersensitivity• systemic anaphylaxis - the allergin is usually

picked up by the blood and the reactions occur throughout the body. Examples include severe allergy to insect stings, drugs, and antisera.

• localized anaphylaxis - the allergin is usually found localized in the mucous membranes or the skin. Examples include allergy to hair, pollen, dust, dander, feathers, and food.

• Disorders - Atopy ( Atopic syndrome ) - Asthma - Anaphylaxis

• The process of anaphylaxis consists of the following sequential events:

First exposure: to an antigen (allergen),such as bee venom, results in production of IgE class of antibodies by plasma cells.The surface of mast cells contains specific receptors

for IgE. IgE molecules are bound to their receptors on the

surface of mast cells and basophils.

• Second exposure: results in binding of the antigen to IgE on the mast cells .This then triggers the release of mast cell

granules, which are :• Histamine -causes constriction of smooth

muscles ( ex bronchioles ), vasodilatation, Increased capillary permeability, increase bronchial mucus secretion.

• Chemotactic factors for eosinophils, proteases.• Leukotrienes -causes bronchial spasms.• Prostaglandins

• Histamine: Dilates and increases permeability of blood vessels (swelling and redness), increases mucus secretion (runny nose), smooth muscle contraction (bronchi).

• Prostaglandins: Contraction of smooth muscle of respiratory system and increased mucus secretion.

• Leukotrienes: Bronchial spasms.– Anaphylactic shock: Massive drop in blood

pressure. Can be fatal in minutes.

Mast Cells and the Allergic Response

2. Antibody-dependent cytotoxicity

• Mechanism: Either IgG or IgM is made against normal self antigens as a result of a failure in immune tolerance, or a foreign antigen resembling some molecule on the surface of host cells enters the body and IgG or IgM made against that antigen then cross reacts with the host cell surface.

The binding of these antibodies to the surface of host cells then leads to:

Opsonization of the host cell. Activation of the classical complement

pathway causing MAC lysis ( membrane attack complex ) of the cells. ADCC (Antibody-Dependent Cell-

Mediated Cytotoxicity ) destruction of the host cells.

Complement system

• It consists of series of proteins synthesised by liver as acute phase reactants.

• 1. Augments host immune defenses• 2.Lysis bacteria directly with MAC (Membrane

attack complex).• 3. Participates in cytotoxic immunity and

immune complex hypersensitivity reactions.

• The multiple activities of the complement system:

• Lysis• Opsonization• Activation of inflammatory response• Clearance of immune complexes

• NOTE;• C3a……….Anaphylotoxin• C3b………..opsonin• C5a………..Anaphylotoxin, Adhesion,

Chemotactic• C5b67…………..Chemotactic complex• C5b6789…………………MAC• MAC; Membrane attack complex

3. Immune complex-mediated

Mechanism: This is caused when soluble antigen-antibody (IgG or IgM) complexes, which are normally removed by macrophages in the spleen and liver, form in large amounts and overwhelm the body . These small complexes lodge in the capillaries, pass between the endothelial cells of blood vessels - especially those in the skin, joints, and kidneys - and become trapped on the surrounding basement membrane beneath these cells.

• The antigen/antibody complexes then activate the classical complement pathway.

Note: This may cause:

Massive inflammation, due to complement protein C5a triggering mast cells to release inflammatory mediators.

Influx of neutrophils , due to complement protein C5a , resulting in neutrophils discharging their lysosomes and causing tissue destruction and further inflammation .

MAC lysis of surrounding tissue cells, due to the membrane attack complex, C5b6789n;

Aggregation of platelets, resulting in more inflammation and the formation of microthrombi that block capillaries;

Activation of macrophages , resulting in production of inflammatory cytokines and extracellular killing causing tissue destruction.

serum sickness, a combination type I and type III hypersensitivity.

autoimmune acute glomerulonephritis. rheumatoid arthritis. systemic lupus erythematosus.the skin lesions of syphilis and leprosy. Arthus reaction. Post streptococcal glomerulonephritis. Lupus Nephritis. Extrinsic allergic alveolitis

(Hypersensitivity pneumonitis)

• Associated disorders:

Delayed hypersensitivity• cell-mediated rather than antibody-

mediated.• T8-lymphocytes become sensitized to an

antigen and differentiate into cytotoxic T-lymphocytes while effector T4-lymphocytes become sensitized to an antigen and produce cytokines . CTLs, cytokines, eosinophils, and/or macrophages then cause harm rather than benefit.

Summary of Hypersensitivity reactionsProduction of antibodies to substances most tolerate, ie allergies.

• Type I (acute) - Most common, starts within seconds and most often ends within 30 minutes.

– Anaphylaxis – causes edema, mucus, and congestion– Asthma – reaction to inhaled allergen.

• Causes massive release of histamine and spasmatic contraction of the bronchioles.

– Anaphylactic shock – systemic response to an injected allergen.

• Can cause bronchiolar constriction, circulatory shock, and possible death.

• Type II (antibody-dependant cytotoxic)- as in transfusion reaction.

• Type III (immune complex)- large antibody-antigen complexes that get trapped under the tunic interna of blood vessels and cause inflammation.

• Type IV (delayed)- occur 12 to 72 hours after exposure. Delay commonly associated with travel time to lymph nodes. Cosmetics and poison ivy hapten commonly do this.

T helper cell function

They help the activity of other immune cells by releasing T cell cytokines. These cells help, suppress or regulate immune responses.

Examples:

- The cell or tissue damage done during diseases like tuberculosis, leprosy, smallpox, measles, herpes infections, candidiasis, and histoplasmosis

- the skin test reactions seen for tuberculosis and other infections.

- contact dermatitis like poison ivy.

- type-1 insulin-dependent diabetes where CTLs destroy insulin-producing cells.

- multiple sclerosis, where T-lymphocytes and macrophages secrete cytokines that destroy the myelin sheath that insulates the nerve fibers of neurons.

- Crohn’s disease and ulcerative colitis.

- psoriasis.

Table 5 - Comparison of Different Types of hypersensitivity

characteristics type-I(anaphylactic)

type-II(cytotoxic)

type-III(immune complex)

type-IV(delayed type)

antibody IgE IgG, IgM IgG, IgM None

antigen exogenous cell surface soluble tissues & organs

response time 15-30 minutes minutes-hours 3-8 hours 48-72 hours

appearance weal & flare lysis and necrosis erythema and edema, necrosis

erythema and induration

histology basophils and eosinophil

antibody and complement

complement and neutrophils

monocytes and lymphocytes

transferred with antibody antibody antibody T-cells

examples allergic asthma, hay fever

erythroblastosisfetalis, Goodpasture's nephritis

SLE, farmer's lung disease

tuberculin test, poison ivy, granuloma

Allergic Contact Dermatitis Response to Poison Ivy Hapten

Autoimmune DiseasesA. Type II (Cytotoxic) Autoimmune ReactionsInvolve antibody reactions to cell surface

molecules, without cytotoxic destruction of cells.– Grave’s Disease:

• Antibodies attach to receptors on thyroid gland and stimulate production of thyroid hormone.

• Symptoms: Goiter (enlarged thyroid) and bulging eyes.– Myasthenia gravis:

• Progressive muscle weakness. Antibodies block acetylcholine receptors at neuromuscular synapse.

• Affects 25,000 Americans (mainly women).• Today most patients survive when treated with drugs or

immunosuppressants.

SLE• Systemic lupus erythematosus, often abbreviated

as SLE or lupus, is a systemic autoimmune disease (or autoimmune connective tissue disease) that can affect any part of the body.

• As occurs in other autoimmune diseases, the immune system attacks the body's cells and tissue, resulting in inflammation and tissue damage.

• It is a type III hypersensitivity reaction in which bound antibody-antigen pairs (immune complexes) precipitate and cause a further immune response.

SLE

• The disease occurs nine times more often in women than in men, especially in women in child-bearing years ages 15 to 35.

LUPUS (SLE)

• Etiology: Antibodies (ABs) directed against the patient’s own DNA, HISTONES, NON-histone RNA, and NUCLEOLUS

• Pathogenesis: Progressive DEPOSITION and INFLAMMATION to immune deposits, in skin, joints, kidneys, vessels, heart, CNS, LIVER.

• Morphology: “Butterfly” rash (NOT discoid), skin deposits, glomerolunephritis.

• Clinical expression: Progressive renal and vascular disease, POSITIVE A.N.A.

INSULIN-DEPENDENT DIABETES MELLITUS (IDDM)

• Synonym• Type I diabetes, DM-type I

• Accounts for 5% to 10% of diabetes in US

• Female to male ratio of 1:1

• Effector mechanisms• CD8 T cells and autoantibodies against beta cells

• Glutamic acid decarboxylase (GAD)• Insulin

PATHOPHYSIOLOGY OF IDDM• Pancreatic beta cells are damaged by

• Infectious agents•Mumps virus, rubella virus, coxsackie

B virus• Toxic chemicals

• Damaged beta cells present antigens which trigger immune attack in genetically susceptible

INSULIN-DEPENDENT DIABETES MELLITUS (IDDM)

• Symptoms• Increased thirst• Frequent urination• Increased hunger• Weight loss• Fatigue

RHEUMATOID ARTHRITIS (RA)• Characterized by inflammation of synovial

membrane of joints and articular surfaces of cartilage and bone

• Involved joints are swollen, warm, painful, and stiff on arising or following inactivity.

• Vasculitis is a systemic complication• Affects 3% to 5% of U.S. population• Female to male ratio of 3:1• HLA DR4 is genetic risk factor

NORMAL Bi-Layered Synovium

↑Destructive Rheumatoid

Synovitis

MULTIPLE SCLEROSIS (MS)

• Chronic unpredictable disease of CNS with four possible clinical causes

• Characterized by patches of demyelination and inflammation of myelin sheath

• Prevalence higher in Northern Hemisphere• North of 37th parallel (125 cases /100,000)• South of 37th parallel (70 cases /100,000)

• Female to male ratio of 2:1

MULTIPLE SCLEROSIS (MS)

• Effector mechanisms• Myelin basic protein is primary

autoantigen for CD4 TH1 cells

• Radiology diagnosis• MRI for detecting demyelinating

lesions (plaques)

Immunodefeciency disorders

• Defect in B- cell, T- cell, complement or phagocytic cells.

• Risk factors• A. prematurity• B. autoimmune diseases• C. lymphoproliferative disorders• D. infections• E. immunosuppressive drugs

ImmunoDefiency Syndromes (-IDS)

• PRIMARY (GENETIC) (P-IDS)• SECONDARY (ACQUIRED) (A-IDS)

PRIMARY

• CHILDREN with repeated, often severe infections, cellular AND/OR humoral immunity problems, autoimmune defects

• B-cell disorders• BRUTON (X-linked agammaglobulinemia)• COMMON VARIABLE• IgA deficiency• T cell disorders• DI GEORGE (THYMIC HYPOPLASIA) 22q11.2• Combined B and T cell disorders• SCID (Severe Combined Immuno Deficiency)• Wiskott Aldrich syndrome• Ataxia telangiectasia

(A)IDS/(SECONDARY IDS)

• Etiology: HIV• Pathogenesis: Infection, Latency, Progressive

T-Cell loss• Morphology: MANY• Clinical Expressions: Infections, Neoplasms,

Progressive Immune Failure, Death, HIV+, HIV-RNA (Viral Load)

• AIDS – Acquired Immunodeficiency diseases

– Acquired after birth, like HIV.– HIV targets helper T cells– Most patients with AIDS die of

opportunisitic infections.

– Opportunistic infection: An infection that occurs because of a weakened immune system. Opportunistic infections are a particular danger for people with AIDS.

– The HIV virus itself does not cause death, but the opportunistic infections that occur because of its effect on the immune system can.